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To evaluate the application of multiple b values diffusion-weighted imaging based on biexponential signal decay model to predict the response to concurrent chemoradiotherapy in cervical cancer patients. This prospective study enrolled 28 patients (mean age: 50.89 ± 10.70 years) with cervical cancer confirmed by biopsy who received concurrent chemoradiotherapy. Pelvic magnetic resonance scans were performed 2 weeks before, 7 days and 21 days after the initiation of therapy, and 1 month after the end of the treatment. Diffusion-weighted imaging with b values of 0, 50, 450, and 850 s/mm2 were performed, and tumor volume, means of tumor apparent diffusion coefficient (ADC)min, ADCmean, ADCslow, ADCfast, and Ffast were measured. Pretreatment ADCmin and ADCslow of good outcome group were significantly higher than those of poor outcome group (P < .05). At the 7th day of the treatment, Ffast and its change rate of good outcome group were significantly higher than those of poor outcome group (P < .05). At the 7th day and 21st day of the treatment, Ffast showed a slowly increasing tendency with no significant difference compared with pretreatment value in poor outcome group (P < .05). One month post-treatment, only ADCslow change rate was significantly higher in good outcome group than that in poor outcome group. Intravoxel incoherent motion-related ADC values could be utilized to better predict the outcome of cervical cancer chemoradiotherapy.

HOXA transcript at the distal tip (HOTTIP), which is a long noncoding RNA, plays an important role in multiple cancers and in coronary artery disease. Elevated microRNA-143 (miR-143) expression causes impaired glucose uptake that is responsible for the ischemic cerebral injury. However, the role and mechanism of HOTTIP in ischemic stroke are still unknown. The expression of HOTTIP and miR-143 was first detected in mouse models of transient middle cerebral artery occlusion and in primary neurons exposed to oxygen-glucose deprivation (OGD). We used gain-of function and loss-of function approaches in vitro to investigate the effect and mechanism of HOTTIP on ischemic stroke by evaluating cell viability, apoptosis, and glycolytic metabolism of neurons exposed to OGD. The HOTTIP expression was decreased, whereas miR-143 increased in experimental ischemic stroke models. Overexpression of HOTTIP by the pcDNA3.1-HOTTIP plasmid significantly increased cell viability, glucose uptake, and the expression of hexokinase 2 (HK-2) and pyruvate kinase M2 that were reduced by OGD insult. The HOTTIP overexpression also diminished OGD induced the apoptosis and the caspase-3 activity of neurons. The miR-143 mimic reversed these effects, and anti-miR-143 enhanced them. In addition, we found that HOTTIP could function as a competing endogenous RNA for miR-143 to modulate HK-2 expression. In conclusion, the HOTTIP expression was reduced in ischemic stroke. The HOTTIP overexpression attenuated OGD-induced neuronal injury and imbalanced glycolytic metabolism by sponging miR-143, resulting in the de-repression of its endogenous target HK-2. Taken together, these findings improve understanding of the pathogenesis of ischemic stroke.

Renal cell carcinoma (RCC) is one of the most common malignancies in the urinary system. Due to the lack of early symptoms, diagnosis of RCC usually occurs at late stages or after cancer metastasis leading to poor prognosis. Therefore, it is crucial to study early molecular mechanisms and biomarkers. Previous studies have suggested that microRNAs are involved in RCC initiation and development, making them a good candidate for early diagnosis and therapy. MiR146b-5P plays important roles in the progression of multiple cancers including thyroid cancer, pancreatic cancer, cervical cancer. However, it is not clear whether and how miR146b-5P is involved in RCC. In this study, we aimed to investigate the function of miR146b-5P in RCC. We examined the expression levels of miR146b-5p in renal cancer tissue and cell lines. We also explored the effects of blocking miR146b-5p in renal tumor growth and inflammatory signaling. Finally, we determined if miR146b-5p regulates tumorigenesis through TRAF6. We found that miR146b-5p levels were significantly increased in renal cancer tissue and renal cancer cells. Blocking miR146b-5p suppressed renal tumor growth and enhanced inflammatory response through increased TRAF6 expression. These effects were eliminated in TRAF6 knockout mice. Our results suggest that enhanced miR146b-5p expression may be a biomarker for RCC and modulating miR146b-5p and TRAF6 levels represent a potential therapeutic strategy for RCC.

Background: Elevated tumor necrosis factor-α (TNF-α) is correlated with refractory Takayasu arteritis (TA), and resistance exercise have been shown to inhibit TNF-α. Hypothesis: We aimed to explore the effect of resistance exercise in the clinical management of TA. Methods: This clinical trial enrolled a total of 342 acute TA patients, who were subsequently randomized to undergo either resistance exercise or relaxation control twice per week for 12 weeks. The disease activity was defined using the primary outcome of Birmingham Vascular Activity Score (BVAS). Secondary outcomes included levels of plasma TNF-α and C-reactive protein (CRP), and the erythrocyte sedimentation rate (ESR). Results: BVAS scores along with other laboratory parameters obtained from the patients in the resistance exercise group showed a gradual decline throughout the course of the trial. By contrast, outcomes appeared largely unaltered in the relaxation control group patients. Analyses also revealed that plasma TNF-α displayed strong linear correlations with ESR, BVAS scores, and plasma CRP levels. Conclusion: Resistance exercise could substantially improve treatment outcomes as well as laboratory parameters in patients with acute TA, probably through decreasing TNF-α.